Recessive genetic mutations of the T-locus in the house mouse affect either the spermatozoan transmission frequencies or the fecundity of males which are heterozygous or homozygous for these mutations. Our data show that these two phenotypic expressions, which are expressions of different sites within the genetic locus, are a result of two separable events. The data suggest that the sterility is caused by a lack of maturation of epididymal spermatozoa, whereas the increased transmission frequency results from a physiological advantage of tn-bearing spermatozoa. The expression of the latter phenotype is both time and environment dependent. Information available from our previous studies will now enable us to further investigate both of these phenotypic expressions of tn-alleles and to correlate these expressions with the mutant gene activity. We will use both in vivo and in vitro techniques in these investigations. Our proposed studies will 1) more fully define the maturational events which the spermatozoa in sterile males do, and do not, undergo during their transit through the mutant epididymides, and 2) compare in vitro, the metabolism of tn-bearing spermatozoa with their transmission frequencies. Our concluded studies will provide 1) a more detailed analysis of factors associated with these two divergent phenotypic effects on male reproduction, and 2) information which will clarify the role of gene action on the events which are responsible for male fertility and for the enhanced transmission frequencies of gametes carrying deleterious mutations.